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J M Varga

Publications and source records attributed to J M Varga.

11 recordsLinked to original sources
PubMed1977

The number of receptors for beta-melanocyte stimulating hormone in Cloudman melanoma cells is increased by dibutyryl adenosine 3':5'-cyclic monophosphate or cholera toxin.

Cultured Cloudman melanoma cells exposed either to dibutyryl 3':5'-cyclic AMP and theophylline or to cholera toxin bind significantly more 125I-labeled beta-melanocyte stimulating hormone (MSH) and fluorescein-labeled MSH than untreated cells. MSH binds to melanoma cells in the G2 phase of the cell cycle. The stimulation of MSH binding by dibutyryl cyclic AMP results from an increase in the number of MSH receptors per G2 cell and, to a lesser extent, from an increase in the number of G2 cells. The affinity of the receptors for MSH is not influenced by dibutyryl cyclic AMP.

Bacterial Toxins↗
PubMed1977

Multispecific lymphoid cell surface receptors.

When mice are sequentially immunized with two antigens to give an oligoclonal "double-binding" antibody response, there is a concomitant increase of "double-binding" cell surface receptors on their splenic lymphocytes. Competition studies suggest that the capacity to bind the two ligands, bovine pancreatic ribonuclease (EC 3.1.4.22) and a 2,4-dinitrophenyl (DNP) derivative, is a function of the same molecules. In ribo-nuclease-primed mice, an early response to bovine gamma globulin containing an average of 60 Dnp groups per molecule is the appearance of an increasing number of cells bearing surface receptors binding both ribonuclease and Dnp. Later, these double-binding cells are diluted by cells that bind Dnp, but not ribonuclease. The analogous phenomenon is observed when the two antigens are used in reverse order. While other reports suggest that there may be several different receptors in relatively undifferentiated cells from unimmunized mice, it seems likely that cells committed to antibody production carry a predominant multispecific cell surface immunoglobulin receptor.

Animals↗
PubMed1976

Nonrandom distribution of receptors for melanocyte-stimulating hormone on the surface of mouse melanoma cells.

An improved bubble method was developed for applying an ultrathin layer of nuclear track emulsion on the surface of cells labeled with I125-MSH. The autoradiographs of I125-MSH binding indicate a nonrandom distribution of receptors on the surface of mouse melanoma cells. It is suggested that MSH receptors are displayed in clusters previous to and independently of their exposure to the hormone.

Acetone↗
PubMed1976

Association of cell surface receptors for melanotropin with the Golgi region in mouse melanoma cells.

Binding of beta-melanotropin (betal-melanocyte stimulating hormone) to mouse melanoma cells occurs in a region on the cell surface overlying the Golgi complex. This association was demonstrated by labeling cells with fluorescein isothiocyanate hormone and by locating the Golgi complex with a histochemical test for thiamine pyrophosphatase activity. The biologically active fluorescent hormone appears on the surface and later in vesicles in the malanized cells, as judged by fluorescence microscopy. It is conceivable that internalization of the hormone is instrumental in the process of hormonally induced melanization. Because initial and late events of hormonally induced pigmentation are related to the Golgi complex, it is likely that instructions that follow the attachment of melanotropin to receptors are carried out in a compartmentalized manner.

Cell Line↗
PubMed1976

Melanocyte-stimulating hormone receptors on cultured guinea-pig melanocytes.

Guinea-pig melanocytes in mixed epidermal cell cultures bind melanocyte-stimulating hormone in a distinct focal surface area in their perinuclear field and thus follow the same pattern previously described for Cloudman melanoma cells. The labeling index ranged from 18 to 34%. Pretreatment of cultures with trypsin leads to destruction of melanocyte-stimulating hormone receptors whereas neuraminidase has no such effect.

Cell Line↗
PubMed1975

Melanoma cells resistant to inhibition of growth by melanocyte stimulating hormone.

Melanocyte stimulating hormone (MSH) enhances melanization but inhibits proliferation of Cloudman S91 melanoma cells in culture. We have isolated variants of these cells that can grow in the presence of MSH. The conclusions we have reached from analyses of these cells are the following: (1) Basal tyrosinase activity (monophenol monooxygenase; monophenol, dihydroxyphenylalanine:oxygen oxidoreductase, EC 1.14.18.1), i.e., the activity that is present in the absence of added MSH, is related through a common biochemical pathway to MSH-mediated control of growth. (2) MSH-inducible tyrosinase activity does not appear to be related to MSH control of growth. (3) The morphological changes that occur following the addition of MSH or cAMP are related to controls of growth and not to those of melanization.

Animals↗
PubMedDate not supplied

Polyfunctional antibodies. Their biology and inheritance.

It seems likely that immunoglobulins have evolved from some archetypal molecule and those forms which are useful to the animal have been retained. It is this entire population of antibodies which forms the humoral immune system and in such a system, not only the properties of individual antibody combining regions, but the properties of the multiprotein system as a whole, are important for the defences of the body against pathogens. Antibody combining sites may bind a disparate set of structurally related and unrelated ligands. This multispecificity can be biologically meaningful: the same clone can be stimulated by different antigens. In this sense, cell surface immunoglobulins are multifunctional. The major biological consequence of antibody multispecificity is overlapping binding functions within subsets of the total antibody repertoire. The most significant impact of this overlap is: (1) it reduces the number of V genes necessary to code for the total number of combining sites; (2) the cross-stimulation of clones by structurally related and unrelated antigens may be instrumental in the normal maintenance of immune responsiveness and in addition, it may explain the ability to respond to unusual and less ubiquitous antigens; (3) the antigenic history of the animal may contribute to the maturation of the immune response by cross-stimulation of pre-selected clones of antigen binding cells.

Animals↗